Presbycusis

Definition and prevalence (how big a problem is presbycusis?)

Presbycusis is the high frequency hearing loss that typically accompanies aging.
Presbycusis has an extremely high prevalence. Self-reported hearing impairment
ranges from 5.4% in 18-44 year old persons to 29.6% in those 65 and older (Schoenborn
and Marano, 1988). The prevalence of hearing impairment on hearing testing is
is high as 83% in people between the age of 57 and 89 (Mosicki et al, 1985).
More detailed data can be found from the government survey result reported here
(pdf file).

The progressive decline in hearing sensitivity generally begins in the third
decade of life. The hearing loss is generally sensorineural and begins at the
higher frequencies. In many cases hearing loss is accompanied by
tinnitus. While hearing can be often improved by hearing
aids, many hearing aid recipients prefer not to use them because electrical
amplification cannot replace natural hearing..

Pathology: What is found when you look at these ears under the microscope

While individuals with presbycusis are generally considered as a monolithic
group, it is possible to split them up. Schuknecht (1993) divided presbycusis
into four pathological subgroups: 1). sensory characterized by hair cell loss
in the basal turn where high-frequency hearing is served 2). Neural, characterized
by spiral ganglion cell loss and disproportionate loss of speech understanding,
3). Stria vascularis loss (vascular), and 4). Conductive (middle ear disease).
However the pattern and severity of cochlear degeneration often do not correlate
well with the level of hearing loss.

Etiology: What causes presbycusis ?

Urban populations appear to have more presbycusis, suggesting that environmental
noise and/or ototoxin exposure
contributes to presbycusis. It also seems likely that genetic factors play a
role in determining susceptibility. For example, certain strains of mice show
a rapid deterioration of hearing function that resemble human hearing loss (Henry
and Chole, 1980; Li, 1994). In humans, a
recent study suggested that heritability of medium and low frequencies was .38
and .31 (DeStefano et al, 2003).

A variety of hypotheses have been advanced to explain this deterioration. A
decline in mitochondrial function is currently a popular hypothesis as the mitochondria
are the powerplants of the cell and there is a well known increase in mitochondrial
DNA mutations with age, associated with a decline in mitochondrial respiratory
function (Liannaine et al, 1989). A strong correlation between mitochondrial
DNA mutations and cell atrophy has been shown in muscle and perhaps this also
applies to the ear. Mitochondrial mutations may cause cell damage because of
inadaquete energy or production of free radicals. The latter are highly reactive
chemicals that are often the product of incomplete oxidative processes. Free
radicals are produced after nearly any type of cellular injury, and are also
produced in the ear.

A second train of evidence relates to programmed cell death or apoptosis. In
general there is a delicate balance in the body between cell death and risk
of damaged cells surviving and consequent neoplasia (cancer). Cell death is
associated with depletion of energy stores and therefore it would be expected
that cells with mutated mitochondrial DNA would be more likely to undergo apoptosis
than normal cells.

Treatment:

The sensorineural component of presbycusis can be treated with hearing
aids, when it is not severe. Conductive type presbycusis can also be treated
with hearing aids but also can sometimes be treated with surgery. Avoidance
of excessive noise and ototoxin exposure is certainly wise in any individual
with hearing loss. There is currently a trend towards recommending of antioxidant
foods and medications over long periods in an attempt to slow the progression
of presbycusis.